There is good evidence that histaminergic neurones can activate H1 receptors in the supra-optic nucleus of the hypothalamus to increase the release of arginine vasopressin. Early key findings (Hough 1988) include high densities of histaminergic fibres and H1 receptors in this area, increases in plasma vasopressin levels following intracerebral HA injections, and antagonism of these effects by H1 blockers. More recent in vitro experiments have confirmed monosynaptic inputs from tuberomammillary neurones to vasopressinergic sur-praoptic cells; activation of the former induces increased dye coupling in the latter, and this effect is inhibited by H1 antagonists (Hatton and Yang 1996). However, an in vivo experiment attempting to demonstrate vasopressin release following tuberomammillary stimulation did not reach the same conclusion (Akins and Bealer 1993). Other in vivo studies in rats have shown that dehydration activates the histaminergic system, and the dehydration-induced stimulation of vasopressin release is reduced by inhibitors of HA synthesis and by H1 antagonists (Kjaer et al. 1994). Interestingly, when the latter experiment was performed in humans, H2 antagonists, but not H1 antagonists, inhibited the vasopressin release. (Kjaer et al. 2000). Histaminergic neurones are also able to activate the synthesis and release of other hypothalamic-hypophyseal hormones, including oxytocin, CRH, ACTH and beta-endorphin; Both H1 and H2 receptors appear to contribute to these effects (Kjaer et al. 1998).

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